Our hypotheses are that the increase in hepatic glucose release in response to a give increment in glucagon is greater in people with non-insulin dependent diabetes mellitus (NIDDM) than in nondiabetic humans indicating enhanced sensitivity to glucagon; and a given increment in glucagon results in a greater percent increase in glycogenolysis in people with NIDDM than in nondiabetic humans. The short-term aim of the proposed studies is to determine whether glucagon has a greater effect on glucose production in people with NIDDM than in nondiabetic subjects. The intermediate term aim of the proposed studies is to develop a qualitative measure of glycogenolysis in humans. The long-term aim of the proposed studies is to develop a method that permits quantitative measurement of glycogenolysis in humans and to use this method along with other existing methods to study the regulation of glycogenolysis, gluconeogenesis and hepatic glucose release in health and disease. We will also measure glucagon's effect on amino acid kinetics in this protocol, since amino acids provide substrate for gluconeogenesis and glucagon has been shown to affect amino acid metabolism